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Tuberculosis

Aug 24, 20255 min read

TB

Dr. Isra

Introduction

Tuberculosis (TB), a disease with a long and complex history, has been known by various names. Initially called “Tabes” due to the wasting and weight loss it caused, it was later dubbed the “white plague” because of the paleness of its victims. Finally, it was shortened to “TB.”

Caused by the bacterium Mycobacterium tuberculosis, TB is transmitted through inhalation and was responsible for countless deaths before the development of antituberculous drugs.

Pathophysiology of Primary TB

  1. Inhalation and Ingestion: Mycobacterium tuberculosis enters the body through inhalation participates in upper lobe due high oxygen - and typically settles in the middle and lower lobes of the lungs. Macrophages, immune cells responsible for engulfing foreign bodies, ingest the bacilli-shaped bacteria to destroy it but fails to do so

  2. Inhibition of Lysosomes: The mycobacterium cleverly inhibits the attachment of lysosomes, cellular components responsible for breaking down foreign materials. This prevents the macrophages from effectively destroying the bacteria.

  3. Intracellular Multiplication: Protected within the macrophages, the mycobacterium begins to multiply.

  4. Cytokine Release: The infected macrophages release signaling molecules called cytokines, specifically IL-1, IL-6, and TNF-alpha. These cytokines attract T helper cells and T cytotoxic-CD8 cells to help the infected MQ to get rid of intracellular pathogens.

Type IV hypersensitivity reaction

  1. Granuloma Formation: T lymphocytes release interferon-gamma, which triggers the formation of a granuloma, a collection of immune cells attempting to contain the infection. Fibrosis occurs around the granuloma, further limiting the spread. This is known as the Ghon focus.

  2. Hilar Lymphadenopathy: The infection often spreads to nearby hilar lymph nodes, leading to their enlargement, a condition called hilar lymphadenopathy.

  3. Ghon’s Complex: The combination of the Ghon focus and hilar lymphadenopathy is referred to as Ghon’s complex, characteristic of primary TB infection.

Fate of Primary TB

  • Remission/Latent TB (90%): In most cases, the immune system successfully contains the infection, leading to remission or latent TB. Calcification and fibrosis occur at the site of infection, forming a structure known as the Ranke complex. (immunocompetent ⇒ Immunosuppressed)

  • Secondary TB (Reactivation): Years later, if immunosuppression develops, latent TB can reactivate, leading to secondary TB.

  • Primary Progressive Disease (immunosuppressed) (10%): In individuals with weakened immune systems, such as those with HIV, diabetes, or organ transplants, the primary infection may progress into active disease. This is known as primary progressive disease typically found in lower lobe of lungs

Secondary and Primary Progressive TB

  • Upper Lobe Involvement: In both secondary and primary progressive TB, the bacteria often spread to the upper lobe of the lungs, where there is more oxygen, as Mycobacterium tuberculosis thrives in oxygen-rich environments.

  • Fibro-cavitation: Bacterial multiplication in the upper lobe causes lung damage and the formation of cavities filled with fibrous tissue (fibro-cavitation).

Clinical Manifestations

General Features; due cytokine release by macrophageZ

  • Fever
  • Night sweats
  • Loss of appetite
  • Weight loss

Pulmonary ManifestationsZ

  • Cough; bronchial tree stimulation cough receptor - due inflammation
  • Hemoptysis (coughing up blood); necrosis bronchial tree, blood vessels
  • Bronchopneumonia; Inflammation and infection of the bronchi and surrounding lung tissue, leading to consolidation and impaired gas exchange.
  • Pleural effusion (fluid buildup around the lungs) + Pneumothorax

Systemic ManifestationsZ TB Mmop

  • CNS: Space-occupying lesions and TB meningitis

  • Neck: Enlarged cervical lymphadenopathy (“scrofula”)

  • Cardio: Constrictive pericarditis (presents with an “egg-shell” appearance on chest X-ray)

  • Liver: Hepatitis

  • Adrenal: Primary adrenal insufficiency

  • Kidney: Pyelonephritis (can lead to sterile pyuria - pus in the urine)

  • Peritoneum: TB peritonitis

  • Bone-Vertebra: Pott’s disease of the spine

  • Long Bones: TB Osteomyelitis

  • Disseminated Infection: When TB spreads through the bloodstream and lymphatics to other organs, it’s called miliary TB.

InvestigationsZ

  • PPD Test (Mantoux, Tuberculin Sensitivity Test): This skin test involves injecting purified protein derivative (PPD) intradermally. Results are read after 48-72 hours.
    • 5 mm: Considered positive in immunosuppressed individuals or those with Sarcoidosis.
    • 10 mm: Diagnostic if the individual has close contact with a TB patient, is a refugee, a prisoner, or a healthcare worker.
    • 15 mm: Considered positive in everyone; diagnostic

False Positives: BCG vaccine can cause a false-positive result. False Negatives: HIV and Sarcoidosis can cause false-negative results. 5mm

  • IFN-Gamma Release Assays (IGRA): Used to differentiate between latent and active TB infection and to rule out false-positive or false-negative PPD results.
  • before giving Infliximab; IBD, Crohns, Rheumatoid - do IGRA

  • Chest X-Ray: Helps differentiate between primary and secondary TB. upper lobe, Ghons lesion, rankes complex

  • Histopathology and Sputum Culture: These are the gold standard investigations for diagnosing TB.

DIFF:

  • Sarcoidosis,
  • Pneumonia
  • Malignancy; Lung Cancer,
  • Vinger; Hemoptysis,
  • aspergilossis,

Anti-Tuberculosis TreatmentsX

Latent TB

Active TB

Directly Observed Therapy (DOT) is crucial for ensuring adherence to treatment.

CorticosteroidsZ

Corticosteroids are administered to TB patients in specific situations and only after initiating anti-TB medication:

  • Adrenal TB: As replacement therapy.
  • TB Meningitis: To prevent adhesions and neurological deficits.
  • Severe Miliary TB
  • TB Pericarditis: To prevent constrictive pericarditis.

Adverse Effects of MedicationsZ

Latent, Active; initial + Continuation

  • Rifampicin:

    • Red-orange discoloration of urine, tears, and sweat.
    • Hepatic enzyme inducer (contraceptive, …)

  • Isoniazid::

    • Peripheral neuropathy (numbness and tingling in the extremities); correction with VIT B6 - slow acetylation
    • Hepatotoxicity (liver damage); fast acetylation

Active; Initial

  • Pyrazinamide:

    • Gouty attacks (joint pain due to uric acid buildup).
    • Hepatotoxicity.

  • Ethambutol:

    • Optic neuritis (inflammation of the optic nerve, potentially leading to vision problems). Ishihara chart is used to monitor for this side effect.

  • Streptomycin:

    • Ototoxicity (hearing loss).
    • Nephrotoxicity (kidney damage).

tactile frem;percussion

  • inc; cavity; hyper-ressonance, consolidation; dull, fibrosis; heterogenous
  • dec;

Graph View

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